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Ketamine has been around for many years. It has recently been getting more attention in the ED for its use as an analgesic, amnestic, sedative, and even for its bronchodilator effects. Are we using it correctly?

How does it work? Ketamine act as an NMDA receptor antagonists. NMDA receptors are voltage gated and ligand gated receptors. They require depolarization and a substrate for activation. Glutamate is the strongest ligand that binds to the receptors and it causes an influx of sodium and calcium and an efflux of potassium, resulting in depolarization. NMDA receptors are thought to play a role in learning and memory, vision, motor control, and neuroprotection. Receptors are found in the hippocampus, cerebral cortex, ventral and dorsal horns of the spinal cord [1]. When ketamine binds to the NMDA receptors it briefly “disconnects” many of the NMDA receptors, causing the anesthetic, amnestic and dissociative effects. Ketamine also acts as a serotonin, dopamine, and norepinephrine reuptake inhibitor resulting in euphoria. The weak agonist effects of the μ-opioid and κ-opioid receptors may also add to this effect. Finally, ketamine improves analgesia due to a decrease in the production of NO, a neurotransmitter involved in pain perception.

Procedural Sedation- Things we know, Ketamine works Newton et al looked at 92 patients requiring procedural sedation over a two-year period and found that 98.8% of patients successfully underwent procedural sedation. Overall, 21.7% had adverse effects including agitation (13%), clonic movements (7%), and four patients had vomiting. They concluded that these adverse events were not significant and ketamine achieved adequate levels of procedural sedation [2]. Strayer et al in Am J Emerg Med reviewed data from older studies (N=87) and found that 10-20% had an “emergence phenomena” [3]. Emergence reactions have been described as awakening from the sedation with extreme agitation often requiring treatment with benzodiazepines. Reports are more common in pediatric patients and incidence ranges from 2% to 50% [4,5]. Miner et al looked at the difference between using Ketamine or Propofol in a randomized clinical trial. He found that recovery agitation was seen more frequently in patients receiving ketamine (36%) than in those receiving propofol (8%). The median time to regain baseline mental status was longer in the ketamine group (14 minutes) versus the propofol group (5 minutes). Overall conclusion was that either were safe and effective. Interestingly, pain was reported by 3 of 50 patients in the propofol group and 1 of 47 patients in the ketamine group (95% confidence interval = -11.9 to 4.1), and some part of the procedure was remembered by 4 of 50 patients in the propofol group and 6 of 47 patients in the ketamine group (95% CI = -7.6% to 17.1%) [6]. Procedural Sedation- Better together: Ketamine and Propofol? In 2007 Loh et al found no difference in hemodynamic or respiratory compromise between “ketofol” and propofol [7]. That same year, Willman et al did a prospective evaluation of "ketofol" (ketamineat 0.75 mg/kg andpropofolat 0.75 mg/kg) for procedural sedation and analgesia in the emergency department (N=114). They found that 96% had successful sedation without adjuncts, 3 had emergence phenomena, recovery was on average 15 minutes, and no one experienced hypotension or vomiting [8]. Thomas et al looked at the combination of ketamine and propofol versus either agent alone for procedural sedation in the emergency department. Patients were given a bolus of ketamine (0.3-0.5-mg/kg), followed by a propofol bolus (0.4-1-mg/kg). Sedation was maintained with intermittent boluses of propofol 0.1-0.5 mg/kg). They concluded that the combined use of ketamine and propofol is a reasonable alternative to propofol alone for procedural sedation in patients at higher risk for respiratory depression or hypotension [9]. Andolfatto et at looked at Ketamine-propofol combination (0.375 mg/kg each of ketamine and propofol) versus propofol alone (0.75 mg/kg of propofol) for emergency department procedural sedation and analgesia in a randomized double-blind trial. They found that there was no difference in adverse respiratory events in the ketofol group compared with the propofol group and that sedation depth appeared to be more consistent with ketofol [10]. The decision to use ketamine, propofol, or “ketofol” depends of the patient history and comorbidities. All three options seem acceptable, and “ketofol” is a safe alternative for those who have underlying respiratory disease or even mild hypotension.The future of Ketamine Treating depression? Use as an adjunct bronchodilator in asthma/COPD? Sedative agent in those who are hypotensive?

In what situations have you been able to maximize ketamine's effectiveness and vast potential?References

I heart Ketamine. Great overview of its uses and citing of the literature to back it up.

Are residents at your program using sub-dissociative doses of ketamine (0.1mg/kg) for agitated or altered patients for ease of imaging ??

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